Volume 5, Issue 2 (Avicenna Journal of Pharmaceutical Research, Dec 2025)
Avicenna J Pharma Res 2025, 5(2): 76-82 |
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Pazandeh M H, Ahadi A M, Doudi M, Nili-Ahmadabadi A. Protective Effect of Chlorogenic Acid on Methyl Methanesulfonate-Induced DNA Damage in Mouse Spleen Tissue. Avicenna J Pharma Res 2025; 5 (2) :76-82
URL: http://ajpr1.umsha.ac.ir/article-1-45-en.html
URL: http://ajpr1.umsha.ac.ir/article-1-45-en.html
1- Medicinal Plants and Natural Products Research Center, Hamadan University of Medical Sciences, Hamadan, Iran & Department of Pharmacology and Toxicology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran
2- Department of Genetics, College of Science, University of Shahrekord, Shahrekord, Iran.
3- Department of Microbiology, Fal. C Islamic Azad University, Isfahan, Iran
4- Medicinal Plants and Natural Products Research Center, Hamadan University of Medical Sciences, Hamadan, Iran. & Department of Pharmacology and Toxicology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran
2- Department of Genetics, College of Science, University of Shahrekord, Shahrekord, Iran.
3- Department of Microbiology, Fal. C Islamic Azad University, Isfahan, Iran
4- Medicinal Plants and Natural Products Research Center, Hamadan University of Medical Sciences, Hamadan, Iran. & Department of Pharmacology and Toxicology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran
Abstract: (54 Views)
Background and Objective: Chlorogenic acid (CGA) is a prominent bioactive compound with diverse pharmacological properties. This study aimed to evaluate the potential protective effects of CGA against methyl methanesulfonate (MMS)-induced genotoxicity in the spleen of male BALB/c mice.
Methods: A total of 36 male BALB/c mice were randomly allocated to six experimental groups (n=6 per group). The control group received normal saline (NS; 1 mL/kg) daily for seven consecutive days. The second group received NS (1 mL/kg) for seven days, followed by a single intraperitoneal (i.p.) injection of MMS (10 mg/kg) one hour after the last NS administration. The third group was treated with CGA (40 mg/kg/day) alone for seven days. The fourth, fifth, and sixth groups were pretreated with CGA at doses of 10, 20, and 40 mg/kg/day, respectively, for seven days; on day 7, one hour after the final CGA dose, each of these groups received a single i.p. injection of MMS (10 mg/kg). Approximately 3 h after MMS injection, all mice were humanely euthanized (ketamine/xylazine), and spleen tissues were collected for subsequent histopathological and biochemical analyses.
Results: MMS treatment significantly increased DNA damage in spleen cells, as indicated by the comet assay, and this genotoxic effect was accompanied by elevated caspase-3/7 activities. Pretreatment with CGA attenuated MMS-induced DNA damage, with reduced DNA migration observed at 10 mg/kg (P<0.05) and 20 mg/kg (P<0.001) CGA doses. CGA also markedly decreased caspase-3/7 activity in spleen tissue at all tested doses. These biochemical findings were supported by histopathological analysis, which showed preservation of normal splenic architecture in the CGA-pretreated groups against MMS-induced damage.
Conclusion: This study demonstrates that CGA protects against MMS-induced genotoxicity in murine spleen tissue. CGA pre-treatment significantly reduced DNA damage and suppressed caspase-3/7 activity, indicating an inhibitory effect on MMS-induced apoptosis. These findings highlight the chemoprotective potential of CGA against genotoxic chemicals.
Methods: A total of 36 male BALB/c mice were randomly allocated to six experimental groups (n=6 per group). The control group received normal saline (NS; 1 mL/kg) daily for seven consecutive days. The second group received NS (1 mL/kg) for seven days, followed by a single intraperitoneal (i.p.) injection of MMS (10 mg/kg) one hour after the last NS administration. The third group was treated with CGA (40 mg/kg/day) alone for seven days. The fourth, fifth, and sixth groups were pretreated with CGA at doses of 10, 20, and 40 mg/kg/day, respectively, for seven days; on day 7, one hour after the final CGA dose, each of these groups received a single i.p. injection of MMS (10 mg/kg). Approximately 3 h after MMS injection, all mice were humanely euthanized (ketamine/xylazine), and spleen tissues were collected for subsequent histopathological and biochemical analyses.
Results: MMS treatment significantly increased DNA damage in spleen cells, as indicated by the comet assay, and this genotoxic effect was accompanied by elevated caspase-3/7 activities. Pretreatment with CGA attenuated MMS-induced DNA damage, with reduced DNA migration observed at 10 mg/kg (P<0.05) and 20 mg/kg (P<0.001) CGA doses. CGA also markedly decreased caspase-3/7 activity in spleen tissue at all tested doses. These biochemical findings were supported by histopathological analysis, which showed preservation of normal splenic architecture in the CGA-pretreated groups against MMS-induced damage.
Conclusion: This study demonstrates that CGA protects against MMS-induced genotoxicity in murine spleen tissue. CGA pre-treatment significantly reduced DNA damage and suppressed caspase-3/7 activity, indicating an inhibitory effect on MMS-induced apoptosis. These findings highlight the chemoprotective potential of CGA against genotoxic chemicals.
Type of Study: Research |
Subject:
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Received: 2026/09/28 | Accepted: 2025/02/28 | Published: 2026/09/28
Received: 2026/09/28 | Accepted: 2025/02/28 | Published: 2026/09/28
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